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. 2022 Apr 27;11(9):1470.
doi: 10.3390/cells11091470.

Expression Profiles of GILZ and Annexin A1 in Human Oral Candidiasis and Lichen Planus

Affiliations

Expression Profiles of GILZ and Annexin A1 in Human Oral Candidiasis and Lichen Planus

Mahmood S Mozaffari et al. Cells. .

Abstract

Adrenal glands are the major source of glucocorticoids, but recent studies indicate tissue-specific production of cortisol, including that in the oral mucosa. Both endogenous and exogenous glucocorticoids regulate the production of several proteins, including the glucocorticoid-induced leucine zipper (GILZ) and Annexin A1, which play important roles in the regulation of immune and inflammatory responses. Common inflammation-associated oral conditions include lichen planus and candidiasis, but the status of GILZ and Annexin A1 in these human conditions remains to be established. Accordingly, archived paraffin-embedded biopsy samples were subjected to immunohistochemistry to establish tissue localization and profile of GILZ and Annexin A1 coupled with the use of hematoxylin-eosin stain for histopathological assessment; for comparison, fibroma specimens served as controls. Histopathological examination confirmed the presence of spores and pseudohyphae for oral candidiasis (OC) specimens and marked inflammatory cell infiltrates for both OC and oral lichen planus (OLP) specimens compared to control specimens. All specimens displayed consistent and prominent nuclear staining for GILZ throughout the full thickness of the epithelium and, to varying extent, for inflammatory infiltrates and stromal cells. On the other hand, a heterogeneous pattern of nuclear, cytoplasmic, and cell membrane staining was observed for Annexin A1 for all specimens in the suprabasal layers of epithelium and, to varying extent, for inflammatory and stromal cells. Semi-quantitative analyses indicated generally similar fractional areas of staining for both GILZ and Annexin A1 among the groups, but normalized staining for GILZ, but not Annexin A1, was reduced for OC and OLP compared to the control specimens. Thus, while the cellular expression pattern of GILZ and Annexin A1 does not differentiate among these conditions, differential cellular profiles for GILZ vs. Annexin A1 are suggestive of their distinct physiological functions in the oral mucosa.

Keywords: Annexin A1; GILZ; human; immunohistochemistry; oral candidiasis; oral lichen planus.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Panels show H&E staining of three tissue specimens from each experimental group confirming presence of marked immune and inflammatory cells in oral candidiasis and oral lichen planus compared to control tissues. Scale bar: 100 μm.
Figure 2
Figure 2
Panel shows image from one tissue specimen stained with PAS to show presence of Candida albicans. Scale bar: 50 μm.
Figure 3
Figure 3
Panels show immunohistochemical staining for GILZ in three tissue specimens from each group of control, oral candidiasis, and oral lichen planus. For each condition, GILZ immunostaining was confined to nuclei. Scale bar: 100 μm.
Figure 4
Figure 4
Panels show immunohistochemical staining for Annexin A1 in three tissue specimens from each group of control, oral candidiasis, and oral lichen planus. Each condition displayed nuclear, cytoplasmic and cell membrane staining for Annexin A1, albeit to varying extent as described under Results. Scale bar: 100 μm.
Figure 5
Figure 5
Panels show GILZ and Annexin A1 staining for one tissue sample from control, oral candidiasis, and oral lichen planus groups at higher magnification to better illustrate staining patterns. While GILZ immunostaining is confined to nuclei, Annexin A1 immunostaining is seen for nuclei, cytoplasm, and cell membrane. Further, sparring of Annexin A1 immunostaining is seen for basal layers of epithelium, although less discernable for OLP but more prominent for OC, compared to control, specimens. Scale bar: 50 μm.
Figure 6
Figure 6
Panel (A) shows fractional area of staining, while panel (B) shows staining normalized to nuclei for proteins of interest. Data are means ± SEM for each condition; n = 5–10 specimens for each condition as indicated under Methods. * p < 0.05 compared to the control group.

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